Evidence map›Paper›PMID 20587524›Full record

ArticleCancer research2010

MicroRNA biogenesis is required for Myc-induced B-cell lymphoma development and survival.

Maria Pia Arrate, Tiffaney Vincent, Jessica Odvody, Rekha Kar, Stephen N Jones, Christine M Eischen

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.8field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

30 citing papers in PubMed, 51 citations in OpenAlex.

  1. Cells · 2025
    Article
  2. Review
  3. MicroRNA-21 is Required for Hematopoietic Cell Viability After Radiation Exposure.International journal of radiation oncology, biology, physics · 2019
    Article
  4. Article
  5. Article
  6. Constitutive Dicer1 phosphorylation accelerates metabolism and aging in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Maria Pia ArrateDepartment of Pathology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA.
Tiffaney Vincent
Jessica Odvody
Rekha Kar
Stephen N Jones
Christine M Eischen
University of Massachusetts Chan Medical School · USVanderbilt University · US

Funding

Tumor Immunology and Microenvironment Research ProgramP30CA068485 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MATTHEW J TYSKA · 1995 to 2026
$172.8M
The Role of MDM Proteins in Cell Growth and TumorigenesisR01CA077735 · NCI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI JONES, STEPHEN, ZHANG, HONG · 1999 to 2019
$5.7M
The Role of Mdm2 in Lymphoma DevelopmentR01CA098139 · NCI · VANDERBILT UNIVERSITY · PI EISCHEN, CHRISTINE M · 2003 to 2007
$1.5M
p53-Independent Pathways in Mdm2-Mediated TransformationR01CA117935 · NCI · VANDERBILT UNIVERSITY · PI EISCHEN, CHRISTINE M. · 2007 to 2011
$1.5M
NCI NIH HHS P30 CA068485NCI NIH HHS P30CA68485NCI NIH HHS R01 CA077735NCI NIH HHS R01CA077735NCI NIH HHS R01 CA098139NCI NIH HHS R01CA098139NCI NIH HHS R01 CA117935NCI NIH HHS R01CA117935
6 · The paper itself

Abstract

Many tumor cells express globally reduced levels of microRNAs (miRNA), suggesting that decreased miRNA expression in premalignant cells contributes to their tumorigenic phenotype. In support of this, Dicer, an RNase III-like enzyme that controls the maturation of miRNA, was recently shown to function as a haploinsufficient tumor suppressor in nonhematopoietic cells. Because the Myc oncoprotein, a critical inducer of B-cell lymphomas, was reported to suppress the expression of multiple miRNAs in lymphoma cells, it was presumed that a deficiency of Dicer and subsequent loss of miRNA maturation would accelerate Myc-induced lymphoma development. We report here that, surprisingly, a haploinsufficiency of Dicer in B cells failed to promote B-cell malignancy or accelerate Myc-induced B-cell lymphomagenesis in mice. Moreover, deletion of Dicer in B cells of CD19-cre(+)/Emicro-myc mice significantly inhibited lymphomagenesis, and all lymphomas that did arise in these mice lacked functional Cre expression and retained at least one functional Dicer allele. Uncharacteristically, the lymphomas that frequently developed in the CD19-cre(+)/Dicer(fl/fl)/Emicro-myc mice were of very early precursor B-cell origin, a stage of B-cell development prior to Cre expression. Therefore, loss of Dicer function was not advantageous for lymphomagenesis, but rather, Dicer ablation was strongly selected against during Myc-induced B-cell lymphoma development. Moreover, deletion of Dicer in established B-cell lymphomas resulted in apoptosis, revealing that Dicer is required for B-cell lymphoma survival. Thus, Dicer does not function as a haploinsufficient tumor suppressor in B cells and is required for B-cell lymphoma development and survival.

Indexed as

Genes, mycAllelesAnimalsCell Transformation, NeoplasticDEAD-box RNA HelicasesEndoribonucleasesGene DeletionGenes, p53Lymphoma, B-CellMiceMice, KnockoutMicroRNAsRibonuclease IIIDEAD-box RNA HelicasesDicer1 protein, mouseEndoribonucleasesMicroRNAsRibonuclease III

Identifiers

PMID20587524
PMCPMC2906119
OpenAlexW2109558380

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.